NEUROBIOLOGICAL ASPECTS OF APHASIA THERAPY
NEUROBIOLOGICAL ASPECTS OF APHASIA THERAPY
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DOI：
10.1080/02687038808248912
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发表时间：
1988-05-01
期刊：
影响因子：
2
通讯作者：
ALBERT, ML
中科院分区：
文献类型：
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作者：
ALBERT, ML
传统上，神经生物学主要是基础神经科学家的兴趣所在，而失语症治疗则是语言病理学家的专利。本文反对这种科学孤立主义。过去十年的基础神经科学和失语症康复研究为基于应用神经生物学的失语症治疗提供了根本不同的方法。在本文中，我首先强调了脑研究中与脑损伤后功能恢复有关的关键发现。接下来，我总结了失语症治疗的新的实验方法的结果。最后，我建议的方式，今天的神经生物学可能适用于治疗失语症的沟通障碍。脑损伤后的功能恢复是一个以爆炸性速度发展的领域。（Laurence and Stein 1978，马歇尔1984，Freed，de Medinacelli and Wyatt 1985，Finger 1978）。遗憾的是，关于功能恢复的脑机制的知识很少专门用于失语症的恢复（Fazzini，Bachman和Albert 1986）。在这一节中，我将讨论脑损伤后失语症的功能恢复。左半球外侧裂周区域的经典“语言区”（Dejerine 1914）通过长和短的联合纤维与左半球的其他区域（包括丘脑和基底神经节）以及右半球的相应区域（Brodal 1981）有着丰富而广泛的联系。语言区内任何地方的损伤都必然会破坏这些远距离区域的功能，尽管那里的神经细胞可能不会受到损伤（Meyer，Shinohara，Kanda，Ericsson and Kok 1970，Metter，里格，Hanson，Carnras，Phelps and Kuhl 1984）。这些远端区域的功能恢复与失语症的语言能力恢复相关（Knopman，Rubens，Selnes，Klassen和Meyer 1984）。因此，药物或环境的调控可以加速代谢受抑制但未受损的神经细胞从功能障碍中恢复，从而加速失语症的恢复。最初，随着组织破坏，在与破坏区域相关的区域中存在局部水肿和远处代谢活性抑制。水肿和血液制品的吸收以及侧支循环的建立导致病变部位的恢复。这个过程需要几个星期。代谢活动的远距离抑制在数月内缓慢恢复。首先，活动在右半球中返回，然后是同侧丘脑和基底神经节，最后是皮质的相邻区域（Fazzini等人，1986年）。失神经超敏反应发展迅速，可能会干扰恢复过程（Langen 1975）。多巴胺能和胆碱能系统的超敏反应在一个月时达到最大值，与临床时间进程平行。
Traditionally, neurobiology has been ofinterest mainly to basic neuroscientists, while aphasia therapy has been the preserve of speech pathologists. This paper argues against such scientific isolationism. Research of the past ten years in basic neuroscience and aphasia rehabilitation has created opportunities for fundamentally different approaches to aphasia therapy, based on applied neurobiology. In this paper I first highlight key findings in brain research relating to recovery of function following brain damage. Next, I summarize results from new, experimental approaches to aphasia therapy. Finally, I suggest ways in which today’s neurobiology may be applied for treatment of communication disorders in aphasia. Recovery of function following brain damage is a field advancing with explosive rapidity.(Laurence and Stein 1978, Marshall 1984, Freed, de Medinacelli and Wyatt 1985 and Finger 1978). Unfortunately, knowledge of brain mechanisms of recovery of function has rarely been applied specifically to recovery from aphasia (Fazzini, Bachman and Albert 1986). In this section I discuss aspects of recovery of function following brain damagc as they apply to aphasia. The classical ‘zone of language’(Dejerine 1914) in the left hemispheric perisylvian region is abundantly and extensively connected via long and short association fibres to other regions of the left hemisphere, including thalamus and basal ganglia, and to corresponding regions of the right hemisphere (Brodal 1981). Damage anywhere within the zone of language will necessarily disrupt function in these distant regions, although nerve cells there may not be damaged (Meyer, Shinohara, Kanda, Fukucchi, Ericsson and Kok 1970, Metter, Riege, Hanson, Carnras, Phelps and Kuhl 1984). Recovery of function in these distant areas has been correlated with recovery of language ability in aphasia (Knopman, Rubens, Selnes, Klassen and Meyer 1984). It follows that pharmacologic or environmental manipulation which can hasten recovery from dysfunction in metabolically suppressed, but undamaged, nerve cells will speed aphasia recovery.When brain tissue has been acutely damaged, recovery follows a characteristic pattern. Initially, with tissue destruction, there is local edema and distant suppression of metabolic activity in regions connected with the area of-destruction. Recovery at the site of lesion results from resorption of Edema and blood products, and establishment of collateral circulation. This process takes several weeks. Recovery from distant suppression of metabolic activity occurs slowly over a period of months. First, activity returns in the right hemisphere, then the ipsilateral thalamus and basal ganglia, finally adjacent regions of cortex (Fazzini el al., 1986). Denervation supersensitivity develops rapidly, and may interfere with processes of recovery (Langen 1975). Supersensitivity is maxim; J for dopaminergic and cholinergic systems at one month, paralleling the time course for the clinical